Work on this project has led to the hypothesis that inhibition of DNA replication triggers induction of a cluster or recA ion lex ion- dependent inducible functions, including filamentous growth, prophage induction and "SOS repair", the error-prone system of postreplication repair of DNA responsible for ultraviolet (UV) mutagenesis in E. coli. We propose: 1) to verify the SOS repair hypothesis, by the use of temperature-sensitive dna and ligase-deficient mutants, by demonstrating "indirect induction" of the SOS repair system, and by isolating mutants constitutive for SOS repair, 2) to determine whether the SOS repair system caused mutations by inaccurate recombinational repair or by a type of repair replication capable of replicating DNA past pyrimidine dimers; 3) to analyze the error-free type of postreplication repair performed by lex strains; 4) to attempt to isolate mutants temperature- sensitive for inducibility of SOS repair and other recA ion lex ion- dependent ("reclex") functions in order to test the hypothesis that all of hese functions are regulated by a common effector; 5) to determine whether UV-mutable derivatives of lex strains are consititutive for SOS repair of for another system of error-prone repair; 6) to isolate tif derivatives in which filamentous growth is no longer thermally inducible, to make possible quantitative study of the mutator activity of SOS repair in tif strains at elevated temperatures; 7) to determine whether 5-bromouracil mutagenesis involves the SOS repair system by the use of isogenic recA, lex and uvrA derivatives of B/r; 8) to determine whether thymineless death depends upon an inducible product; 9) to determine the possible role of the dnaB product in excision repair; 10) to determine action spectra for induction of several types of mutations in Uvr ion strains, and 11) to investigate the repair requirements of specialized structures in DNA (replication forks, membrane attachment sites) by studying prestarvation effects on survival after UV irradiation in wild type and repair-deficient strains.